Abstract MP69: Relationships Between Sleep Apnea, Cardiovascular Disease Risk Factors, and Aortic Pulse Wave Velocity over 9 Years: The Wisconsin Sleep Cohort
Background: Cardiovascular disease (CVD) risk factors associated with obstructive sleep apnea (OSA) contribute to endothelial dysfunction and arterial stiffening. We hypothesized that OSA severity would predict aortic pulse wave velocity (PWV) after nearly a decade of aging in the Wisconsin Sleep Cohort (WSC).
Methods: Subjects were 596 participants in the WSC that underwent overnight polysomnography between 2000 and 2008; subsequent tonometry data was acquired a mean of 8.8 (standard deviation, 2.1) years later. OSA severity was described by the apnea-hypopnea index (AHI), mean and minimum nocturnal blood oxygen saturation level (SaO2, %), and time with SaO2<90%. AHI+1 was log transformed. Participants using positive airway pressure therapy (PAP) at the tonometry visit were evaluated as a distinct categorical variable. Non-invasive applanation tonometry was used to derive aortic (carotid-to-femoral) PWV. Multivariable linear and logistic regression models that included CVD risk factors, antihypertensive, and lipid medications were fit to evaluate longitudinal associations between baseline OSA markers and future PWV.
Results: At baseline, the 596 participants were mean 55.9 (7.3) years old (53% male, 97.5% Caucasian). Their mean body-mass index (was 31.4 (6.9) kg/m2, 89 (14.9%) had diabetes mellitus, and 252 (42.3%) were hypertensive. Excluding the 40 CPAP users, the mean AHI was 5.8 (7.6) events/hour (range 0.0-53.6); 54 (9.1%) had AHI ≥15 events/hr. Mean SaO2was 94.7% (2.1%) and minimum SaO2 was 82.8% (9.5%). Time with SaO2<90% did not predict PWV. In models adjusted for age and sex, lower mean SaO2 (β=-0.16, SE 0.06, p=0.004), lower minimum SaO2 (β=-0.04, SE 0.01, p=0.005) and higher log10(AHI+1) (β=0.55, SE 0.20, p=0.005) predicted higher PWV a mean of approximately 9 years after OSA assessment. However, none of these associations were statistically significant after waist circumference (p≤0.005 for all 3 outcomes) and height were added to the models. For models with mean SaO2, waist circumference independently predicted PWV, but after addition of CVD risk factors, only age (β=0.14, SE 0.01, p<0.001), systolic blood pressure (β=0.02, SE 0.01, p<0.001), and diabetes status (β=0.96, SE 0.28, p=0.002) were independent predictors. Very similar results were observed for models with minimum Sa02and PWV. None of the OSA parameters interacted with age or smoking status to predict PWV. Presence of Metabolic Syndrome did not predict PWV; it did not interact with OSA parameters to predict PWV.
Conclusions: The longitudinal associations between OSA and PWV are confounded by body size and influenced by diabetes mellitus and blood pressure. These results suggest that weight management and blood pressure control may help prevent arterial stiffening associated with sleep apnea.
Author Disclosures: R. Stern: None. C.E. Korcarz: None. P.E. Peppard: None. J.H. Barnet: None. E.W. Hagen: None. T. Young: None. J.H. Stein: None.
- © 2015 by American Heart Association, Inc.